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Biomedical subjects

U Rafałowska

Publications and source records attributed to U Rafałowska.

30 records · Page 2Linked to original sources
PubMed1987

Enhanced potassium-stimulated gamma-aminobutyric acid release by astrocytes derived from rats with early hepatogenic encephalopathy.

Bulk-isolated astrocytes from rats with early hepatogenic encephalopathy (HE) induced with thioacetamide responded to the increase of potassium in the incubation medium from 5 mM to 75 mM with a markedly enhanced release of previously taken up [14C]gamma-aminobutyric acid ([14C]GABA). The process was not affected by omission of calcium and/or addition of EGTA to the incubation medium. Only a slight stimulation of GABA release by high potassium was observed in astrocytes from control rats. In contrast, histamine and histidine were vigorously released from control astrocytes in high-potassium medium, and their release was not enhanced by HE, indicating that the observed phenomenon is specific for GABA.

Animals↗
PubMed1986

Consequences of exposure of rats to hyperoxygenation for actomyosin-like protein from synaptosomes of brain.

This paper describes the changes caused by in vivo hyperoxygenation of rats in the brain synaptosomal actomyosin-like protein preparation. We demonstrate that this preparation is composed of protein and phospholipid components attached to each other. Upon hyperoxygenation, a peroxidation of phospholipids in the lipid component proceeds. Simultaneously, with the increase of malondialdehyde, conjugated double bonds, and fluorescence intensity levels, a decrease of protein -SH groups levels, and Mg2+-dependent ATPase activity is observed. The above changes reduce the ability of the protein to superprecipitate, which reflects a contractile reaction in vivo.

Actomyosin↗
PubMed1979

Transport of malate and citrate into rat brain mitochondria under hypoxia and anesthesia.

Hypoxia and anesthesia inhibited penetration of malate and citrate into the brain mitochondria by 60% and 40%, respectively. Anesthetized animals exposed to low oxygen tension showed similar changes as those subjected to hypoxia without anesthesia. Recovery from anesthesia was rapid and the rates of citrate and malate uptake returned to the control values in approximately 60 min. In the case of hypoxia, days were required to restore the control values of citrate and malate uptake. Free fatty acids had no effect on the entry of malate and citrate into the mitochondria. However, changes in the levels of protein --SH groups were observed which may be responsible for the impaired transport of citrate and malate under hypoxic condition.

Anesthesia↗
PubMedDate not supplied

Does lead provoke the peroxidation process in rat brain synaptosomes?

Up to now there has been no information concerning the effect of lead on the peroxidation process in brain nerve endings. We have examined whether lead acetate (in chronic and acute models of toxicity in vivo and in vitro) affected the level of free radicals in synaptosomes obtained from rat brain. Simultaneously, we have checked the effect of peroxidation of Pb2+ on brain homogenates and microsomal fraction. Our results indicated that the lead level in synaptosomal fraction obtained from lead-treated rats was much higher than in controls. We did not observe induction of spontaneous and Fe(3+)-dependent peroxidation either in synaptosomes or in homogenates and brain microsomes after chronic and acute lead administration to the rats. Lead itself also did not enhance both processes when added in vitro to the control brain synaptosomes in micromolar concentrations. The lack of the lead effect on the peroxidation process in subcellular fractions of brain was rather surprising, because lead is known to be the accelerator of Fe(3+)-dependent peroxidation processes in liver. Additionally, livers from rats under the same toxicity conditions were examined. We have found that lead did not provoke spontaneous peroxidation in liver, but contrary to brain fractions, it drastically increased iron-dependent peroxidation in liver homogenates and microsomes. The lack of the effect of lead on inducing peroxidation processes in brain is probably the consequence of the brain having stronger protective mechanisms against its toxicity than the liver.

Acute Disease↗